Exaggerated cardiovascular responses to stress may increase one's risk for hypertension and atherosclerosis. Biobehavioral models of the relationship between stress reactivity and cardiovascular disease assume that the perception of stressful events and the translation of stressor perceptions into cardiovascular responses are mediated by a central nervous system network that regulates both cardiovascular and cognitive/emotional states. Thus, processes that trigger potentially pathogenic cardiovascular stress responses are believed to be initiated within the central nervous system. Few studies in humans, however, have examined the central pathways that regulate cardiovascular stress responses. In the present study, functional magnetic resonance imaging (fMRI) will be used to test the hypotheses that (a) patterns of cardiovascular reactivity to laboratory stressors correlate with the activation of brain areas that are presumably involved in both cardiovascular control and cognitive/emotional processes, and (b) that a difference exists in the stressor-induced activation of these brain regions between a group of individuals who have previously demonstrated exaggerated cardiovascular stress reactivity and a group of individuals who have previously demonstrated attenuated cardiovascular reactivity. Results from this study are expected to enhance our understanding of the central control of cardiovascular stress responses, which may influence an individual's cardiovascular risk profile.